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Published on: July 13, 2019
The biology of JC polyomavirus
Abstract:
JC polyomavirus (JCPyV) is the causative agent of a fatal central nervous system demyelinating disease known as progressive multifocal leukoencephalopathy (PML). PML occurs in people with underlying immunodeficiency or in individuals being treated with potent immunomodulatory therapies. JCPyV is a DNA tumor virus with a double-stranded DNA genome and encodes a well-studied oncogene, large T antigen. Its host range is highly restricted to humans and only a few cell types support lytic infection in vivo or in vitro. Its oncogenic potential in humans has not been firmly established and the international committee on oncogenic viruses lists JCPyV as possibly carcinogenic. Significant progress has been made in understanding the biology of JCPyV and here we present an overview of the field and discuss some important questions that remain unanswered.
Insights
JC polyomavirus (JCPyV) causes progressive multifocal leukoencephalopathy (PML), a fatal brain disease in immunocompromised individuals. This overview explores JCPyV biology, its oncogenic potential, and remaining research questions in PML pathogenesis.
Area of Science:
- Virology
- Neuroscience
- Oncology
Background:
- JC polyomavirus (JCPyV) is a human DNA virus responsible for progressive multifocal leukoencephalopathy (PML), a severe demyelinating disease of the central nervous system.
- PML predominantly affects individuals with compromised immune systems or those undergoing immunosuppressive therapies.
- JCPyV possesses an oncogene, the large T antigen, and is classified as possibly carcinogenic, although its oncogenic role in humans is not definitively established.
Purpose of the Study:
- To provide a comprehensive overview of the current understanding of JC polyomavirus biology.
- To discuss the pathogenesis of progressive multifocal leukoencephalopathy (PML) linked to JCPyV infection.
- To highlight critical unanswered questions and future research directions in the field of JCPyV and PML.
Main Methods:
- Literature review and synthesis of existing research on JC polyomavirus.
- Analysis of JCPyV's genomic features, including its oncogenic large T antigen.
- Discussion of host-virus interactions and cellular tropism relevant to JCPyV infection.
Main Results:
- JCPyV exhibits a restricted host range, primarily infecting humans.
- The virus's double-stranded DNA genome and oncogenic potential are key features.
- Significant advancements have been made in understanding JCPyV's biology and its association with PML.
Conclusions:
- JC polyomavirus remains a significant etiological agent of PML in susceptible populations.
- Further research is necessary to fully elucidate JCPyV's oncogenic mechanisms and its role in human disease.
- Addressing knowledge gaps in JCPyV biology is crucial for developing effective therapeutic strategies against PML.
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